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FGF1 - a new weapon to control type 2 diabetes mellitus

kokhongw

Well-Known Member
Messages
2,394
Location
Singapore
Type of diabetes
I reversed my Type 2
Treatment type
Diet only
https://www.researchgate.net/public...ew_weapon_to_control_type_2_diabetes_mellitus
Abstract
A hypercaloric diet combined with a sedentary lifestyle is a major risk factor for the development of insulin resistance, type 2 diabetes mellitus (T2DM) and associated comorbidities. Standard treatment for T2DM begins with lifestyle modification, and includes oral medications and insulin therapy to compensate for progressive β-cell failure. However, current pharmaceutical options for T2DM are limited in that they do not maintain stable, durable glucose control without the need for treatment intensification. Furthermore, each medication is associated with adverse effects, which range from hypoglycaemia to weight gain or bone loss. Unexpectedly, fibroblast growth factor 1 (FGF1) and its low mitogenic variants have emerged as potentially safe candidates for restoring euglycaemia, without causing overt adverse effects. In particular, a single peripheral injection of FGF1 can lower glucose to normal levels within hours, without the risk of hypoglycaemia. Similarly, a single intracerebroventricular injection of FGF1 can induce long-lasting remission of the diabetic phenotype. This Review discusses potential mechanisms by which centrally administered FGF1 improves central glucose-sensing and peripheral glucose uptake in a sustained manner. Specifically, we explore the potential crosstalk between FGF1 and glucose-sensing neuronal circuits, hypothalamic neural stem cells and synaptic plasticity. Finally, we highlight therapeutic considerations of FGF1 and compare its metabolic actions with FGF15 (rodents), FGF19 (humans) and FGF21.

FGF1 - a new weapon to control type 2 diabetes mellitus (PDF Download Available). Available from: https://www.researchgate.net/public...ew_weapon_to_control_type_2_diabetes_mellitus [accessed Feb 27 2018].

 
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kokhongw said:
compensate for progressive β-cell failure
Click to expand...

I assume that means the pancreas function is deteriorating. Pleased to say that in my case, now in my 21st year since T2 diagnosis, having just had my 4th c-peptide blood test in 2 years, my pancreas still seems to be ticking over nicely. I do believe that if I had continued taking Gliclazide and Januvia I would certainly be looking at insulin therapy. In fact my GP was beginning to discuss that option when I started my low carb diet 4 years ago. Just some personal anecdotes.
 
Im also in my 21st year since diagnosis in March 97 and have been on a stable dose of gliclazide throughout apart from an initial period on an insulin pump ( a big beast by todays standards that sat on a trolly behind my hospital bed and had to be wheeled around if I went walkies) but with dietary modifications that reflect that my carb tolerance has gone from 35-40g per meal to under 50g per day
I get a certain perverse pleasure from reading the received wisdom that over 50% of type 2 ‘s on Gliclazide will be on insulin within 6 years and over 75% on multiple drugs within 8.
Confounding received medical truths has been my hobby for years
Never had a c peptide but am planning to request that at next weeks review with my endocrinology consultant
 
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This is a very interesting lecture by Dr Michael Schwarz

The results of 1 FGF1 injection to the brain of the mouse...
 
Oddly there seems to have been little discussion about FGF1 since...
 
kokhongw said:
Oddly there seems to have been little discussion about FGF1 since...
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It seems the original report was an article in Nature, which is a periodical not noted for its sound scientific reporting. A web search of FGF1 does not bring up much useful corroborating evidence of proper research confirming the claims in that article.

Personally I found nothing to give me confidence in this research.
 
I wasn't sure that I fancied someone sticking a needle in my brain to fix something I have sorted out with diet alone...Or is that a misleading graphic?

Also statements like this

"With no widely effective treatment, let alone cure, available and rates of the disease continuing to rise alongside costs, the toll of T2DM seems to be unyielding."

"A hypercaloric diet combined with a sedentary lifestyle is a major risk factor for the development of insulin resistance, type 2 diabetes mellitus (T2DM) and associated comorbidities."

Seem to show a lack of understanding of the causes of Type 2 and the effectiveness of a low carb diet.
 
bulkbiker said:
Or is that a misleading graphic?
Click to expand...

The graphics are correct. The 2 separate studies showed that one shot of FGF1 to the brain of mouse/rats have long lasting effects. While peripheral injections needs to be done on a more regular basis...
 
kokhongw said:
The graphics are correct. The 2 separate studies showed that one shot of FGF1 to the brain of mouse/rats have long lasting effects. While peripheral injections needs to be done on a more regular basis...
Click to expand...
In that case I'd far rather eat roast pork belly for life!
 
I wonder if FGF1 is somehow greatly increased thru regular fasting...
 
bulkbiker said:
Something that Novo Nordisk will never wonder about I bet...
Click to expand...

I am sure they will work on a weekly or monthly injectable version of FGF1 pretty soon. I can almost hear the cash register ringing...kaching, kaching, kaching...
 
kokhongw said:
I am sure they will work on a weekly or monthly injectable version of FGF1 pretty soon. I can almost hear the cash register ringing...kaching, kaching, kaching...
Click to expand...
I have a confession to make.. my cousin works for them.. I'll ask him if he has heard anything about this monstrosity..
 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4718082/

"FGF1 is downstream of PPARγ, a well-known target for the thiazolidinedione (TZD) class of anti-diabetic drugs, leading to the hypothesis that FGF1 mediates a subset of PPARγ-activated genes, and by doing so improves the metabolic profile. Indeed, it has been shown that pharmacological administration of FGF1 normalized blood glucose levels within an hour in obese, diabetic rodents. Chronic administration resulted in normoglycemia, insulin sensitization, and reduced hepatosteatosis (fatty liver). The acute blood glucose lowering effect seems to be dependent on FGFR1 signaling in WAT, since WAT-specific deletion of this factor abrogated FGF1-induced normoglycemia in obese, hyperglycemic mice. Whether the other metabolic improvements (i.e., reduction of hepatic steatosis) are dependent on WAT signaling is unknown"
 
The first reference above is the same Nature article being placed into archive. However, it is a properly reported study report, not a pseudo science blog.

The Salk Institute are mainly interested in insulin dependance diabetes, This study uses those poor mice again, specially made diabetic by either a massively force fed monster fat diet. Usually this type of research uses a standardised mouse for their experiments, where the mice are specially bred for particular damaged gene to assist in induction of diabetes, This model does not correlate too well with the human genome, and so these results may not be transferrable to humans. We have seen that problem arise in similar research that did not actually end in useful human scale products.

Secondly, they blasted a batch of mice with a chemical concoction that killed off the beta cells, and then used them to prove that the FGF1 had no effect, so that would appear to remove the possibility of this being useful to an insulin dependant PWD.

The other thing the report mentions en passante is that the giving of FGF! was followed by a reduction in appetite , a reduction in feeding, and consequent weight loss. But this was not deemed relevant to the study. Those here following the ND diet and LCHF know full well that weight reduction and adipose fat reduction are implicated in improving bgl control (alleged) and so it may be that this treatment will be more like a one shot ND replacement therapy and an answer to a slimmers prayer.

Edit to add: The second report uses the same ob/ob mice models, but does establish that the weight loss due to loss of appetite was not a significant contributor to the effect. It also showed that the single injection does have a prolonged effect (up to 18 weeks at least when monitoring terminated). So it does seem that there is potential in this as a possible treatment for T2D. However, it seems to prove in a way that T2D is all in the mind, in that the injection must be direct to the brain for the effect to be durable. But then FGF1 IS the brain growth hormone after all.
 
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Following on with my comment, I have found the following snippet:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413509/
 
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